SCREENING-LEVEL HAZARD CHARACTERIZATION OF HIGH PRODUCTION VOLUME CHEMICALS SPONSORED CHEMICAL 2,2-Dichloro-l,l?l-trifluoroethane (CAS No. 306-83-2) [9th CI Name: Ethane, 2,2-dichloro-l,l?l-trifluoro-] August 2007 Prepared by High Production Volume Chemicals Branch Risk Assessment Division Office of Pollution Prevention and Toxics Environmental Protection Agency 1200 Pennsylvania Avenue, NW Washington, DC 20460-0001 ------- SCREENING-LEVEL HAZARD CHARACTERIZATION OF HIGH PRODUCTION VOLUME CHEMICALS The High Production Volume (HPV) Challenge Program1 is a voluntary initiative aimed at developing and making publicly available screening-level health and environmental effects information on chemicals manufactured in or imported into the United States in quantities greater than one million pounds per year. In the Challenge Program, producers and importers of HPV chemicals voluntarily sponsor chemicals; sponsorship entails the identification and initial assessment of the adequacy of existing toxicity data/information, conducting new testing if adequate data do not exist, and making both new and existing data and information available to the public. Each complete data submission contains data on 18 internationally agreed to "SIDS" (Screening Information Data Set1'2) endpoints that are screening-level indicators of potential hazards (toxicity) for humans or the environment. The Environmental Protection Agency's Office of Pollution Prevention and Toxics (OPPT) is evaluating the data submitted in the HPV Challenge Program on approximately 1,400 sponsored chemicals. OPPT is using a hazard- based screening process to prioritize review of the submissions. The hazard-based screening process consists of two tiers described below briefly and in more detail on the Hazard Characterization website3. Tier 1 is a computerized sorting process whereby key elements of a submitted data set are compared to established criteria to "bin" chemicals/categories for OPPT review. This is an automated process performed on the data as submitted by the sponsor. It does not include evaluation of the quality or completeness of the data. In Tier 2, a screening-level hazard characterization is developed by EPA that consists of an objective evaluation of the quality and completeness of the data set provided in the Challenge Program submissions. The evaluation is performed according to established EPA guidance2'4 and is based primarily on hazard data provided by sponsors. EPA may also include additional or updated hazard information of which EPA, sponsors or other parties have become aware. The hazard characterization may also identify data gaps that will become the basis for a subsequent data needs assessment where deemed necessary. Under the HPV Challenge Program, chemicals that have similar chemical structures, properties and biological activities may be grouped together and their data shared across the resulting category. This approach often significantly reduces the need for conducting tests for all endpoints for all category members. As part of Tier 2, evaluation of chemical category rationale and composition and data extrapolation(s) among category members is performed in accord with established EPA2 and OECD5 guidance. The screening-level hazard characterizations that emerge from Tier 2 are important contributors to OPPT's existing chemicals review process. These hazard characterizations are technical documents intended to support subsequent decisions and actions by OPPT. Accordingly, the documents are not written with the goal of informing the general public. However, they do provide a vehicle for public access to a concise assessment of the raw technical data on HPV chemicals and provide information previously not readily available to the public. The public, including sponsors, may offer comments on the hazard characterization documents. The screening-level hazard characterizations, as the name indicates, do not evaluate the potential risks of a chemical or a chemical category, but will serve as a starting point for such reviews. In 2007, EPA received data on uses of and exposures to high-volume TSCA existing chemicals, submitted in accordance with the requirements of the Inventory Update Reporting (IUR) rule. For the chemicals in the HPV Challenge Program, EPA will review the IUR data to evaluate exposure potential. The resulting exposure information will then be combined with the screening-level hazard characterizations to develop screening-level risk characterizations4'6. The screening-level risk characterizations will inform EPA on the need for further work on individual chemicals or categories. Efforts are currently underway to consider how best to utilize these screening-level risk characterizations as part of a risk- based decision-making process on HPV chemicals which applies the results of the successful U.S. High Production Volume Challenge Program and the IUR to support judgments concerning the need, if any, for further action. 1 U.S. EPA. High Production Volume (HPV) Challenge Program; http://www.epa.gov/chemrtk/index.htm. 2 U.S. EPA. HPV Challenge Program - Information Sources; http://www.epa.gov/chemrtk/pubs/general/guidocs.htm. 3 U.S. EPA. HPV Chemicals Hazard Characterization website (http://www.epa.gov/hpvis/abouthc.html). 4 U.S. EPA. Risk Assessment Guidelines; http://cfpub.epa.gov/ncea/raf/rafguid.cfm. 5 OECD. Guidance on the Development and Use of Chemical Categories; http://www.oecd.org/dataoecd/60/47/1947509.pdf. 6 U.S. EPA. Risk Characterization Program; http://www.epa.gov/osa/spc/2riskchr.htm. 2 ------- SCREENING-LEVEL HAZARD CHARACTERIZATION 2,2-Dichloro-l,14-trifluoroethane (CAS No. 306-83-2) Introduction The sponsor, DuPont Chemical Company, submitted a Test Plan and Robust Summaries to EPA for 2,2-dichloro- 1,1,1-trifluoroethane (CAS No. 306-83-2; 9th CI name: ethane, 2,2-dichloro-l,l,l-trifluoro-) onDecember 19, 2001. EPA posted the submission on the ChemRTK HPV Challenge website on January 24, 2002 (http://www.epa.gov/chemrtk/pubs/summaries/dicliloro/cl3403tc.htm). EPA comments on the original submission were posted to the website on August 12, 2002. Public comments were also received and posted to the website. This screening-level hazard characterization is based primarily on the review of the test plan and robust summaries of studies submitted by the sponsor(s) under the HPV Challenge Program. In preparing the hazard characterization EPA considered its own comments and public comments on the original submission as well as the sponsor's responses to comments and revisions made to the submission. A summary table of SIDS endpoint data with the structure(s) of the sponsored chemical(s) is included in the appendix. The screening-level hazard characterization for enviromnental and human health toxicity is based largely on SIDS endpoints and is described according to established EPA or OECD effect level definitions and hazard assessment practices. Summary-Conclusion The log Kow of 2,2-dichloro-l,l,l-trifluoroethane indicates that its potential to bioaccumulate is expected to be low. 2,2-Dichloro-l,l,l-trifluoroethane is not readily biodegradable, indicating it has the potential to persist in the environment. The evaluation of available aquatic toxicity data for fish, aquatic invertebrates and aquatic plants indicates that the potential acute hazard of 2,2-dichloro-l,l,l-trifluoroethane to aquatic organisms is low. Acute oral and inhalation toxicity of 2,2-dichloro-1,1,1 -trifluoroethane in rats and acute dermal toxicity in rats and rabbits is low. Following repeated inhalation exposure in rats for 2 years, target organs for toxicity included the liver, pancreas, adrenals, testes and retina. Treatment-related effects seen at the lowest concentration included altered clinical chemistry parameters, lower body weight and body weight gain, higher liver weights, increased incidence of neoplastic and non-neoplastic morphological changes and higher hepatic peroxisomal -oxidation. In a 2-generation reproduction study, the liver was also the target of toxicity as evidenced by altered serum chemistry, increased liver weight and histopathological lesions (hepatocellular enlargement and vacuolation). Decreased implantations count occurred at higher concentrations than the systemic liver effects. Maternal toxicity was seen in developmental toxicity studies in rats and rabbits (i.e., weight loss, clinical signs). Developmental effects were not observed. 2,2-Dichloro-1,1,1 -trifluoroethane did not show a potential to induce gene mutation in bacterial cells. 2,2-Dichloro-1,1,1 -trifluoroethane induced chromosome aberrations in human lymphocytes in vitro, but did not produce chromosome aberrations in rats or increase micronucleus formation in mice following in vivo exposure. Due to the positive findings reported for chromosome aberrations in human lymphocytes, there is a potential concern for genetic toxicity for 2,2-dichloro-l,l,l-trifluoroethane. The potential health hazard of 2,2-dichloro-1,1,1 -trifluoroethane is high based on the results of repeated-dose inhalation toxicity and systemic effects in the F0 animals in the 2-generation reproductive toxicity study. Available data suggest 2,2-dichloro-1,1,1 -trifluoroethane also has genotoxic potential. No data gaps were identified under the HPV Challenge Program. 1. Physical-Chemical Properties and Environmental Fate A summary of physical-chemical properties and enviromnental fate data submitted is provided in the Appendix. For the purpose of the screening-level hazard characterization, the review and summary of these data was limited to the 3 ------- octanol-water partition coefficient and biodegradation endpoints as indictors of bioaccumulation and persistence, respectively. Octanol-Water Partition Coefficient Log Kow: 2.3 (estimated) Biodegradation In a Closed-Bottle Test using an activated sludge as inoculum 2,2-dichloro-l,l,l-trifluoroethane degraded 24% after 28 days. 2,2-dichlo ro-1,1,1-trit'luorocthanc is not readily biodegradable. Conclusion: The log Kow of 2,2-dichloro-l,l,l-trifluoroethane indicates that its potential to bioaccumulate is expected to be low. 2,2-Dichloro-l,l,l-trifluoroethane is not readily biodegradable, indicating it has the potential to persist in the environment. 2. Environmental Effects - Aquatic Toxicity Acute Toxicity to Fish Rainbow trout (Salmo gairdneri) were exposed to 2,2-dichloro-l,l,l-trifluoroethane at nominal concentrations of 13.3, 23.5, 42.5, 74.3 or 133 mg/L for 96 hours under semi-static exposure conditions in a closed system. At 74.3 and 133 mg/L (nominal concentrations), all fish exhibited effects within 4 hours, including darkened pigmentation, lethargic behavior and loss of coordination. At 13.3, 23.5 and 42.5 mg/L (nominal concentrations), 2, 3 and 4 fish were affected by the end of the test, exhibiting either darkened pigmentation or lethargic behavior. 96-h LC50 = 55.5 mg/L Acute Toxicity to Aquatic Invertebrates Daphnia magna were exposed to 2,2-dichloro-l,l,l-trifluoroethane at nominal concentrations of 3.47, 6.94, 13.9, 27.7 or 55.2 mg/L for 48 hours in sealed vessels under static conditions. Effect concentrations were based on immobilization. The lowest mean measured concentration (2.24 mg/L) resulted in 5% immobilization and the highest mean measured value (44.0 mg/L) caused 100% immobilization after 48 hours. 48-h ECS0=17.3 mg/L Toxicity to Aquatic Plants Green algae, Pseudokirchneriella subcapitata were exposed to nominal concentrations of 13.3, 42.5, 133, 425 or 1327 mg/L of 2,2-dichloro-l,l,l-trifluoroethane for 72 hours. Measured concentrations were low compared to nominal values. The two highest concentrations produced a decrease in biomass (mean measured concentrations of 56.3 and 169 mg/L). EC50 for biomass and growth were calculated. 72-h EC50 (biomass) = 67.8 mg/L 72-h EC50 (growth) = 96.6 mg/L Conclusion: The evaluation of available aquatic toxicity data for fish, aquatic invertebrates and aquatic plants indicates that the potential acute hazard of 2,2-dichloro-l,l,l-trifluoroethane to aquatic organisms is low. 4 ------- 3. Human Health Effects Acute Oral Toxicity Male Charles River-CD rats (one per dose group) were given a single dose of 2250, 3400, 5000, 7500, 9000, 11,000, 13,934 or 15,024 mg/kg-bw of 2,2-dichloro-l,l,l-trifluoroethane in corn oil by oral gavage. Rapid respiration and prostration preceded death in rats given a single dose of 9000 mg/kg-bw or greater. Rapid, shallow respiration and prostration (belly-to-cage posture) were observed on the day of dosing in rats given doses of 3400, 5000 or 7500 mg/kg-bw. Acute lethal dose (ALD) was calculated. ALD = 9,000 mg/kg-bw Acute Inhalation Toxicity Six male Charles River-CD rats per group were exposed to vapor concentrations of 20, 700, 32,000, 33,700, 42,100, 52,500 or 55,000 ppm of 2,2-dichloro-l,l,l-trifluoroethane for 4 hours. Mortality ratios for these concentrations were 0/6, 3/6, 3/6, 6/6 and 6/6, respectively. Five minutes after exposure, rats showed a loss of mobility, lethargy, prostration, unresponsiveness to sound and dyspnea. Rats that survived recovered. 4-h LC50 = 32,000 ppm (approximately 200 mg/L) Acute Dermal Toxicity Male and female Crl:CD BR rats (5/sex) and New Zealand White rabbits (5/sex) were exposed to a single dose of 2,2-dichloro-l,l,l-trifluoroethane for 24 hours at 2000 mg/kg-bw and observed for 14 days. No animals died within the 14-day observation period. Nasal or ocular discharge was observed in a single male and female rat. Body weight losses were observed 1 day after treatment (< 12% of initial weight in rats, < 2% of initial weight in rabbits). Dermal irritation was not seen in rats; however, a slight to moderate erythema was seen in 6 of 10 rabbits on the day after treatment (not evident after 5 days). No gross pathological abnormalities were seen in rats or rabbits. LDS0 > 2000 mg/kg-bw Repeated-Dose Toxicity In a 2-year inhalation study, groups of male and female Crl:CD BR rats (80/sex) were exposed (whole-body) to 2,2- dichloro-l,l,l-trifluoroethane at concentrations of 300, 1000 or 5000 ppm (approximately 1.9, 6.25 or 31.25 mg/L/day) for 6 hours/day, 5 days/week for 104 weeks. Effects were observed at all dose levels. Survival was increased at 1000 and 5000 ppm due to a decrease in the incidence of spontaneous lesions in aging rats (glomerulonephropathy). Clinical signs of toxicity observed at 1000 and 5000 ppm included stained fur, wet perineum and wet inguen (i.e., groin). Lower body weight was seen in female rats at 300 ppm and male and female rats at 1000 and 5000 ppm. Clinical chemistry changes occurred at all exposure concentrations and included decreased serum triglycerides, cholesterol, glucose and globulin and increased serum albumin. Urine volume was higher and urine osmolality was lower in treated male rats. Increased liver weight was seen at 5000 ppm. Non- cancer histopathological lesions were seen in the liver, pancreas, adrenals, testes and retina. Tumors were observed in the liver, pancreas, and testes. Male and female rats exposed to 1000 and 5000 ppm had increased hepatic peroxisomal -oxidation activity, indicating an induction of hepatic peroxisome proliferation. LOAEL = 300 ppm (approximately 1.9 mg/L/day; based on effects in clinical chemistry parameters, body and liver weight changes, increased incidence of morphological changes and higher hepatic peroxisomal (3-oxidation activity) NOAEL = Not established Reproductive Toxicity In 2-generation inhalation study, Charles River CD rats (32/sex/F0 generation and 28 rats/sex/ F, generation) were exposed to 2,2-dichloro-l,l,l-trifluoroethane at concentrations of 0, 30, 100, 300 or 1000 ppm (approximately 0.19, 0.625, 1.9 or 6.25 mg/L/day) of for 6 hours/day, 7 days/week (6 weeks of age through weaning for F0; 4 weeks of age through weaning for Fi). Decreased body weight gain was seen in F0 and Fi treated rats. The liver was a target organ, with altered clinical chemistry (e.g., decreased very low density lipoprotein (VLDL), and increased cholesterol profile) and increased liver weight observed at 30 ppm in the F0 animals. Histopathological changes in 5 ------- the liver (i.e., centrilobular hepatocellular enlargement and vacuolation) were seen at 100 ppm and higher. Mating and fertility parameters were not affected by treatment in either generation. Decreased implantation counts were seen in Fi females exposed to 1000 ppm. Impaired pup growth was observed at all concentrations in the offspring of the Fi rats. LOAEL (systemic toxicity) = 30 ppm (approximately 0.19 mg/L/day; based on increased liver weights, slight changes in biochemical parameters) LOAEL (reproductive toxicity) = 1000 ppm (approximately 6.25 mg/L/day, based on decreased implantation counts) NOAEL (reproductive toxicity) = 300 ppm Developmental Toxicity (1) Female New Zealand White rabbits were exposed via inhalation (whole-body) to 2,2-dichloro-l,l,l- trifluoroethane at concentrations of 0, 500, 1500 or 5000 ppm (approximately 3.1, 9.3 or 31.2 mg/L/day) for 6 hours/day during gestation days 6-18. Maternal effects (weight loss, decreased food consumption) were observed at all dose levels. No treatment-related effects on reproductive capacity were observed. No developmental effects were observed. LOAEL (maternal toxicity) = 500 ppm (approximately 3.1 mg/L/day; based on weight loss) LOAEL (developmental toxicity) > 5000 ppm NOAEL (developmental toxicity) = 5000 ppm (2) Female Charles Rivers-CD Albino rats were exposed via inhalation (whole-body) to 2,2-dichloro-l,l,l- trifluoroethane at 0 or 10,000 ppm (approximately 62.5 mg/L/day) for 6 hours/day during gestation days 6-15. Maternal body weight gain was similar to controls. Clinical signs of toxicity during the early phase of the study included lack of coordination and reduced activity and responsiveness to noise. No treatment-related effects on reproductive capacity were observed. No developmental effects were noted. LOAEL (maternal toxicity) = 10,000 ppm (approximately 62.5 mg/L/day; based on a lack of coordination and reduced responsiveness to noise) LOAEL (developmental toxicity) > 10,000 ppm (approximately 62.5 mg/L/day) NOAEL (developmental toxicity) = 10,000 ppm (approximately 62.5 mg/L/day) Genetic Toxicity - Gene Mutation In vitro In a bacterial reverse mutation assay, Salmonella typhimurium strains TA1535, TA1537, TA1538, TA98 and TA100 were exposed to the test substance at concentrations of 0, 0.01, 0.02, 0.05, 0.1, 0.25 or 0.5 mL/vessel, with and without metabolic activation. Cytotoxicity seen at the highest concentration. Positive controls responded as expected. 2,2-Dichloro-l,l,l-trifluoroethane was not mutagenic in this assay. Genetic Toxicity - Chromosomal Aberrations In vitro An in vitro chromosomal aberrations test with 2,2-dichloro-l,l,l-trifluoroethane was conducted in human lymphocytes for 3 hours with and without metabolic activation (concentrations of 0, 7.5, 15 and 30% v/v) and for 24 hours without metabolic activation (concentrations of 0, 2.5, 5 and 10%). Exposure for 3 hours in the absence of metabolic activation produced minor increases in the frequency of aberrant metaphases (p < 0.05 for 7.5%; p < 0.01 for 30%), but only when gaps were included in the analysis. A 3-hour exposure with metabolic activation produced a larger increase in the frequency of aberrant metaphases, both including and excluding gaps (p < 0.001 for 30%) and an increase in the number of polyploid cells. Exposure for 24 hours in the absence of activation produced dose- related, biologically and statistically significant increases in the frequency of aberrant metaphases at all concentrations tested, both including and excluding gaps (p < 0.01 at 2.5% and p < 0.001 at 5 and 10%). No effect on the number of polyploid cells was observed under these conditions. The cytogenetic analyses of the 2.5 and 10% treatment groups were based on two cultures with a total of 200 metaphase cells, respectively. 2,2-Dichloro-l,l,l-trifluoroethane induced chromosomal aberrations in this assay. 6 ------- In vivo (1) In an in vivo chromosomal aberration assay, male Sprague Dawley rats (10/treatement) were treated with a single 6-hour inhalation exposure of 2,2-dichloro-l,l,l-trifluoroethane at concentrations of 0, 300, 1000 or 5000 ppm. Negative findings were reported. 2,2-Dich lo ro-1,1,1-trifluorocthanc did not induce chromosomal aberrations in this assay. (2) In a mouse micronucleus assay, NMRI mice (15/sex) were exposed to concentrations of 0, 2000, 6000 or 18,000 ppm of 2,2-dichloro-l, 1,1-trifluoroethane for 6 hours. Negative findings were reported. 2,2-Dich lo ro-1,1,1-trit'luorocthanc was not mutagenic in this assay. Additional Information Skin Irritation Skin irritation was not observed in any treated male and female New Zealand White rabbits following a 24-hour dermal exposure. No skin irritation was not observed in any treated male albino guinea pigs. Eye Irritation The test substance produced mild to moderate conjunctival irritation with no corneal or iiitic involvement in an unwashed eye of albino rabbits. Sensitization Skin sensitization was not observed in any treated male albino guinea pigs. Conclusion: Acute oral and inhalation toxicity of 2,2-dichloro-1,1,1-trifluoroethane in rats and acute dermal toxicity in rats and rabbits is low. Following repeated inhalation exposure in rats for 2 years, target organs for toxicity included the liver, pancreas, adrenals, testes and retina. Treatment-related effects seen at the lowest concentration included altered clinical chemistry parameters, lower body weight and body weight gain, higher liver weights, increased incidence of neoplastic and non-neoplastic morphological changes and higher hepatic peroxisomal (3-oxidation. In a 2-generation reproduction study, the liver was also the target of toxicity as evidenced by altered serum chemistry, increased liver weight and histopathological lesions (hepatocellular enlargement and vacuolation). Decreased implantations count occurred at higher concentrations than the systemic liver effects. Maternal toxicity was seen in developmental toxicity studies in rats and rabbits (i.e., weight loss, clinical signs). Developmental effects were not observed. 2,2-Dichloro-l,l,1-trifluoroethane did not show a potential to induce gene mutation in bacterial cells. 2,2-Dichloro-1,1,1-trifluoroethane induced chromosome aberrations in human lymphocytes in vitro, but did not produce chromosome aberrations in rats or increase micronucleus formation in mice following in vivo exposure. Due to the positive findings reported for chromosome aberrations in human lymphocytes, there is a potential concern for genetic toxicity for 2,2-dichloro-l, 1,1-trifluoroethane. The potential health hazard of 2,2-dichloro-l, 1,1-trifluoroethane is high based on the results of repeated-dose inhalation toxicity and systemic effects in the F0 animals in the 2-generation reproductive toxicity study. Available data suggest 2,2-dichloro-1,1,1-trifluoroethane also has genotoxic potential. 4. Hazard Characterization The log Kow of 2,2-dichloro-l, 1,1-trifluoroethane indicates that its potential to bioaccumulate is expected to be low. 2,2-Dichloro-1,1,1-trifluoroethane is not readily biodegradable, indicating it has the potential to persist in the environment. The evaluation of available aquatic toxicity data for fish, aquatic invertebrates and aquatic plants indicates that the potential acute hazard of 2,2-dichloro-1,1,1-trifluoroethane to aquatic organisms is low. 7 ------- Acute oral and inhalation toxicity of 2,2-dichloro-1,1,1 -trifluoroethane in rats and acute dermal toxicity in rats and rabbits is low. Following repeated inhalation exposure in rats for 2 years, target organs for toxicity included the liver, pancreas, adrenals, testes and retina. Treatment-related effects seen at the lowest concentration included altered clinical chemistry parameters, lower body weight and body weight gain, higher liver weights, increased incidence of neoplastic and non-neoplastic morphological changes and higher hepatic peroxisomal -oxidation. In a 2-generation reproduction study, the liver was also the target of toxicity as evidenced by altered serum chemistry, increased liver weight and histopathological lesions (hepatocellular enlargement and vacuolation). Decreased implantations count occurred at higher concentrations than the systemic liver effects. Maternal toxicity was seen in developmental toxicity studies in rats and rabbits (i.e., weight loss, clinical signs). Developmental effects were not observed. 2,2-Dichloro-1,1,1-trifluoroethane did not show a potential to induce gene mutation in bacterial cells. 2,2-Dichloro-1,1,1-trifluoroethane induced chromosome aberrations in human lymphocytes in vitro, but did not produce chromosome aberrations in rats or increase micronucleus formation in mice following in vivo exposure. Due to the positive findings reported for chromosome aberrations in human lymphocytes, there is a potential concern for genetic toxicity for 2,2-dichloro-l,l,l-trifluoroethane. The potential health hazard of 2,2-dichloro-1,1,1-trifluoroethane is high based on the results of repeated-dose inhalation toxicity and systemic effects in the F0 animals in the 2-generation reproductive toxicity study. Available data suggest 2,2-dichloro-1,1,1-trifluoroethane also has genotoxic potential. 5. Data Gaps No data gaps were identified under the HPV Challenge Program. 8 ------- APPENDIX Summary Table (if the Screening Information Data Set as submitted under the U.S. HPV Challenge Program Endpoints SPONSORED CHEMICAL 2,2-Dichloro-l,l,l-tritluoroethane (306-83-2) Structure CI F r~i CI F Summary (if Phvsical-Chemical Properties and Environmental Fate Data Melting Point (°C) -107 Boiling Point (°C) 27.8 Vapor Pressure (hPa at 25°C) 941 Log K„w 2.3 Water Solubility (mg/L at 25°C) 2100 Direct Photodegradation Indirect (OH ) Photodegradation Half-life (t1/2) 479 days calculated using a measured rate constant of 3.35*10"14 cm3/molecule-sec. Stability in Water (Hydrolysis) Half-life (t1/2) 13 years at pH 8 and 130 years at pH 7 (estimated) Fugacity (Level III Model) Air (%) Water(%) Soil (%) Sediment (%) 99.8 < 1 < 1 < 1 Biodegradation at 28 days (%) 24 Not readily biodegradable. Summary of Environmental Effects - Aquatic Toxicity Data Fish 96-h LCsn (mg/L) 55.5 Aquatic Invertebrates 48-h ECsn (mg/L) 17.3 Aquatic Plants 72-h ECS0 (mg/L) (biomass) (growth) 67.8 96.6 Summary of Human Health Data Acute Oral Toxicity LDS0 (mg/kg-bw) Acute Dermal Toxicity LDS„ (mg/kg-bw) 9,000 > 2,000 Acute Inhalation Toxicity LC50 (mg/L/6h/day) 32,000 ppm (200 mg/L) 9 ------- Summary Table (if the Screening Information Data Set as submitted under the U.S. HPV Challenge Program Endpoints SPONSORED CHEMICAL 2,2-Dichloro-l,l,l-trifluoroethane (306-83-2) Repeated-Dose Toxicity NOAEL/LOAEL (mg/kg-bw/day) LOAEL = 300 ppm (approximately 1.9 mg/L/day, 2- yr study) LOAEL = 30 ppm (approximately 0.19 mg/L/day, parental toxicity in 2-gen study) Reproductive Toxicity Positive Developmental Toxicity Negative Genetic Toxicity - Gene Mutation In vitro Negative Genetic Toxicity - Gene Mutation In vivo Genetic Toxicity - Chromosomal Aberrations In vitro Positive Genetic Toxicity - Chromosomal Aberrations In vivo Negative Additional Information Skin irritation Eye irritation Sensitization Not irritating Mild to moderate Not sensitizing - indicates endpoint was not addressed for this chemical. 10 ------- |